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Endocrinology, Vol 124, 1571-1575, Copyright © 1989 by Endocrine Society
ARTICLES |
HC Lee, S Bonner-Weir, GC Weir and JL Leahy
Research Division, Joslin Diabetes Center, Boston, Massachusetts.
The aim of the present study was to determine if compensatory adaptions in pancreatic B-cell mass and/or function occur when B-cell mass is reduced without altering glucose tolerance. Islet mass and insulin secretory responses (both in vivo and in vitro) were assessed 19 days after a 40% pancreatectomy (Px) in 5-week-old rats. Plasma glucose and insulin values were unchanged by the 40% Px, both in the fed state and after ip glucose. Also, glucose potentiation of arginine-induced insulin secretion was fully intact when assessed with the in vitro perfused pancreas. Islet mass, assessed using point-counting morphometrics, was 84% of the sham value, not the expected 60%. In contrast, there was no compensatory change in acinar tissue, as judged by pancreatic weight. To determine if the insulin secretory reserve capacity was reduced after the 40% Px, dexamethasone was given on days 14-18. On day 18, the Px rats were midly hyperglycemic, but by the next day, glucose tolerance post-ip glucose was normal, and the insulin responses to the ip glucose in vivo and arginine in vitro were identical in the dexamethasone-treated Px and sham rats. These data show no discernible change in quantitative or qualitative B-cell secretory responses after 40% Px. A key mechanism contributing to this maintenance of normal function was regrowth of much of the excised islet tissue.
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